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Welcome to PSR's Environmental Health Policy
Institute, where we ask questions -- then we ask the experts to
answer them. Join us as physicians, health professionals,
and environmental health experts share their ideas, inspiration, and
analysis about toxic chemicals and environmental health policy.

In avoiding exposures to toxicants in the developing fetus, I
believe our goal should be to be proactive and preventive. We should take into
account all three trimesters as well as periods of continuing neonatal
development into infancy and early childhood. We should not have to be reactive
to widespread damage found years after a toxicant has entered the environment.
This is especially true for those toxicants which are persistent and
bioaccumulative in reproductive aged females. These stored toxicants are
released during pregnancy along with the fat stores required to nourish and
supply energy to the fetus.

There are a number of long recognized important reasons why
children in all stages of development are more susceptible to the toxic effects
of environmental chemicals of many classes. These include mechanisms that
increase both exposure and risk: rapid cell reproduction rates; sensitive
periods of development for different organ systems; greater surface areas in
skin, lungs, and intestinal mucosa per unit of body weight (so that more
toxicants are absorbed per unit of body weight); immature liver and kidney
enzyme systems to metabolize, conjugate, and eliminate toxicants; undeveloped
blood brain barrier so that transport into the brain occurs in the fetus and
child, but not in the adult brain. Additionally, behaviors of the infant and
toddler -- such as being close to the ground where concentrations of toxicants
in air and dust are greater, hand to mouth behaviors, and drinking more fluids
and eating more food per unit of body weight -- all lead to greater exposure
and therefore greater risk of damage from a variety of toxicants. And of course
a longer “shelf life” gives more time to develop diseases. This is suggested by
recent epigenetic explanations of prenatal exposure as a possible mechanism for
determining later adult disease patterns.

All of these mechanisms of increased exposure and absorption
are made worse by socioeconomic conditions which include poverty and poor
nutrition. If the nutritional status of the infant is compromised and there is
inadequate intake of protein, calcium, and iron, for example, the absorption of
toxic substances such as lead is increased. Secondly, a high fat diet increases
exposures to toxicants which are absorbed by and with fat and stored there.

Can we estimate how much of any given toxicant is found in
the bodies of our children? Biomonitoring studies now make it possible to start
to quantify the exposure. However, national epidemiological studies such as
NHANES from the CDC have data only for children over 6. Cord blood monitoring
could give data on a large scale, as this is the least invasive method of
measuring what exposures actually have been during early development.

Prenatal exposures to some toxicants have been firmly linked
to known negative reproductive effects. Well-documented examples include the
relationship between sulfur dioxide in air and cardiac birth defects, and
arsenic exposures associated with severe congenital malformations. Other
pollutants have been measured in air samples at levels associated with adverse
reproductive effects such as premature birth and growth retardation with
decreases in birth length, weight, and head circumference. And an increasing
body of evidence indicates that there are measurable neurodevelopmental and
cognitive effects of early exposures to environmental toxicants.

New human epidemiological studies on prenatal exposures to
estrogenic endocrine disruptors are showing associations with early puberty in
girls, feminization of male children, and decreases in fertility of both men
and women later in life. Exposures to some pesticides, some phthalates, BPA,
and perfluorochemicals are being shown to contribute to male testicular
dysgenesis syndrome, including increasing birth defects such as undescended
testicles and hypospadias, and, later in life, poor semen quality, decreased
fertility, and testicular cancer.

Other endocrine disrupting toxicants such as lead, mercury,
some phthalates, triclosan, PCBs, and PBDEs are associated with disruption of
thyroid hormones in epidemiological studies. In children, of course, thyroid
hormone is truly critical to normal development of all kinds.

These are all areas in which research has begun to reveal
serious problems for the developing human in a polluted environment.

Comments

Constance Simo said ..

Hopefully such a clear and well referenced summary of necessarily outsized detrimental effects of environmental toxins on unborn and developing children, appreciated by the scientific community for decades now, should prompt lawmakers to begin to do something about it. How does the PSR plan to reach the lawmakers? constance.simo@gmail.com